An effective drug sensitizing agent increases gefitinib treatment by down regulating PI3K/Akt/mTOR pathway and up regulating autophagy in non-small cell lung cancer.
We report for the first time significant differences in dynamic signaling between colorectal cancer and NSCLC cell lines exposed to clinically relevant equimolar concentrations of the pan-PI3K inhibitor pictilisib including a lack of reduction of p-AKTser473 in colorectal cancer cell lines (<i>P</i> = 0.037) and lack of compensatory increase in p-MEK in NSCLC cell lines (<i>P</i> = 0.036).
Notably, miR‑802 was able to deactivate the phosphoinositide 3‑kinase (PI3K)/AKT serine/threonine kinase (Akt)/mammalian target of rapamycin (mTOR) pathway in NSCLC cells in vitro and in vivo.
The present study investigated the effects of a PI3K inhibitor on NSCLC growth in bone and osteoclast formation, and aimed to determine whether it could control symptoms associated with bone metastasis.
Our results suggest that miR-503 inhibits NSCLC progression by targeting PDK1/PI3K/AKT pathway, potentiating the use of miR-503 as a biomarker and therapeutic target for NSCLC.
In conclusion, XH002 is a potent oral PI3K/mTOR dual inhibitor that possesses excellent antitumor efficacy against PIK3CA mutant NSCLC, including which resistant to EGFR-TKIs treatments.
Pretreatment with RAD001 (0.1 nmol/L) enhanced the radiosensitivity in NCI-H661 cells with wild-type PIK3CA and KRAS but not in NCI-H460 cells with mutant PIK3CA and KRAS; the sensitivity enhancement ratios in the two NSCLC cell lines were 1.40 and 1.03, respectively.
Thus, our results highlight a compensatory survival mechanism via the MET/STAT3 signaling pathway after PI3K/AKT signaling inhibition in non-small cell lung cancer.
Therefore, inhibition of the PI3K/Akt/mTOR signaling pathway and ERCC1 expression is a potential approach for the treatment of patients with advanced NSCLC.
In summary, Pec was able to inhibit cell proliferation, promote apoptosis and suppress metastasis in NSCLC cells through the PTEN/PI3K/AKT signaling pathway, indicating that Pec is a potential agent for NSCLC therapy.
<b>Conclusions:</b> PI3K/Akt/HIF-1α may contribute to the progression of HPV-associated NSCLC <i>via</i> mediating the expression of EMT-related transcription factors in NSCLC cells.